To the Editor:
I read with interest the article by Rogers and Hew-Butler concerning exercise-associated hyponatremia.
1
While one might dispute whether it constitutes “the most important medical problem of endurance exercise,” exercise-associated hyponatremia clearly presents a serious diagnostic and treatment challenge, particularly in the wilderness environment. Front-line treatment consists of hypertonic saline infusion, yet this may not be readily available or easily administered in all field conditions. Similar limitations apply to the monitoring of serum sodium deemed necessary to manage this treatment.1
, 2
Also, hypertonic saline administration carries risk of complications nearly as severe as hyponatremia.2
These authors and others
1
, 2
, 3
note that inappropriately excessive arginine vasopressin (AVP, also known as antidiuretic hormone or ADH) secretion contributes significantly to the pathophysiology of exercise-induced hyponatremia by limiting aquaresis. Alcohol (ethanol) is a well-established and potent inhibitor of AVP secretion, and circulating AVP is rapidly catabolized.4
, 5
Therefore, I write primarily to hypothesize that oral ethanol consumption may provide a hyponatremia treatment alternative worth investigation. Due to the necessity of limiting water intake with hyponatremia, hard liquor (∼40% ethanol) offers the most medically logical mode of administration. A moderate dose may prove effective (0.5 mL ethanol per kg body weight, or about 2–3 shots of 80 proof liquor), yet only research confirms such matters. The need for sodium intake suggests tequila shots with the customary salt and citrus. The idea offers several advantages: hard liquor is often brought along for recreational purposes even in remote situations, oral consumption requires no intravenous line, moderate oral ethanol imposes no risks comparable to those of intravenous hypertonic saline, and serum sodium monitoring to avoid overcorrection of hyponatremia becomes much less important.As long as it is not overzealous, ethanol consumption may deserve investigation as a treatment alternative for exercise-associated hyponatremia.
References
- Exercise-associated hyponatremia: overzealous fluid consumption.Wilderness Environ Med. 2009; 20: 139-143
- The treatment of hyponatremia.Semin Nephrol. 2009; 29: 282-299
- Exercise-associated hyponatremia.Semin Nephrol. 2009; 29: 271-281
- Direct effects of ethanol on the nervous system.Fed Proc. 1975; 34: 1930-1941
- Endocrine effects of alcohol.Clin Endocrinol Metab. 1978; 7: 351-367
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- Reply to Dr Watenpaugh's LetterWilderness & Environmental MedicineVol. 21Issue 3
- PreviewWe are most grateful for Dr Watenpaugh's interest in this topic, a novel—but currently untested—treatment suggestion. If inappropriately elevated plasma arginine vasopressin concentrations ([AVP]p) are indeed the primary pathophysiological mechanism underlying exercise-induced hyponatremia (EAH),1 then ethanol ingestion would likely suppress AVP during and immediately following exercise.2 The downside of this treatment option is that it would likely take at least an hour before an ethanol-induced diuresis is initiated.
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